Tannerella forsythia (Tf) is a Gram-negative bacterium implicated in various forms of periodontitis and endodontic infections. It remains a relatively less studied periodontal pathogen despite its strong association with oral and systemic diseases. Tf has been thought to be a non- motile organism. However, contrary to this view, we have discovered that the organism is indeed motile and possesses unique ability to glide over solid surfaces ? a type of motility known as gliding motility. Furthermore, genome mining analyses revealed that Tf also possesses homologs of a set of gliding motility proteins present in the bacterium Flavobacterium johnsoniae, a model gliding organism. For instance, the genes coding for the homologs of adhesion proteins SprA/B and RemA as well as the type IX secretion system (T9SS) proteins GldJ, GldK, GldL, GldM, and GldN that form the motility apparatus in F. johnsoniae are present in Tf. Therefore, we hypothesize that despite having no discernable propulsive organelles, such as a flagellum, on its cell surface Tf possesses a gliding motility apparatus and that its gliding motility contributes to its pathogenicity. Herein, we propose two specific aims to define the mechanism of gliding motility and its potential role in the pathogenicity. In Aim 1, we will confirm if Tf has gliding motility using an approach of genetics and biophysics. In Aim 2, we will use in vitro models to assess the role of gliding motility of Tf in biofilm formation and migration through the epithelial layer by comparing the wild-type and motility defective mutants. This R21 exploratory funding mechanism will provide us a unique and timely opportunity to define the underlying mechanisms of motility in Tf in detail. In addition, the findings will contribute to the basic understanding of T9SS regulatory system in gliding motility function in a broad range of bacteria, and the knowledge might lead to designing small molecule inhibitors targeting bacterial motility to intervene periodontitis.